STEPTRACKERHEMATOLOGY + ONCOLOGY | PATHOLOGY | HIGH-YIELD REVIEW

Acute Leukemias

Blasts take over the marrow (> 20%) — abrupt anemia, bleeding and infection. ALL in children, AML in older adults.

FOCUS ON
Tell lymphoid from myeloid: TdT (ALL) vs MPO + Auer rods (AML). Know the prognostic translocations: t(12;21) good and t(9;22) bad in ALL; t(15;17) APL causes DIC and is treated with ATRA. Down syndrome raises risk of both, and tumor lysis syndrome follows treatment.
TYPE
CELL · MARKERS
GENETICS · SUBTYPES
CLINICAL CLUE
Acute leukemia — basics
> 20% blasts in marrow crowd out normal cells.
Maturation arrest in a stem or progenitor cell
Fatigue (anemia), petechiae (↓ platelets), infections (↓ neutrophils), bone pain, organomegaly
B-ALL
children 2–5
Lymphoblasts: TdT⁺, CD10⁺, CD19⁺, CD22, CD79a.
Good: t(12;21) ETV6-RUNX1, hyperdiploidy · poor: t(9;22) (adults), KMT2A/MLL t(4;11) (infants)
Most common childhood cancer; CNS and testes are sanctuary sites → intrathecal therapy
T-ALL
adolescent boys
TdT⁺, CD1a, CD2, CD3, CD5, CD7.
Lymphoblastic lymphoma when a mass dominates
Anterior mediastinal (thymic) mass → SVC syndrome, stridor
AML — basics
older adults
Myeloblasts: MPO⁺, CD13, CD33, CD34, CD117; Auer rods.
Good: t(8;21), inv(16), NPM1 · poor: FLT3-ITD, complex karyotype
Risk: prior alkylators/topoisomerase inhibitors, radiation, benzene, Down syndrome, MDS/MPN
APL (AML-M3)
emergency
Abnormal promyelocytes packed with Auer rods ("faggot cells").
t(15;17) PML-RARA → maturation block at promyelocyte
DIC · all-trans retinoic acid + arsenic trioxide; differentiation syndrome risk; good prognosis
Acute monocytic (M5)
Monoblasts: nonspecific esterase ⁺, often MPO⁻.
—
Gum infiltration, leukemia cutis
Acute megakaryoblastic (M7)
Megakaryoblasts: CD41, CD61; MPO⁻.
GATA1 in Down syndrome
Down syndrome child < 5 years; marrow fibrosis
Myeloid sarcoma
Solid mass of myeloblasts outside the marrow.
May precede or accompany AML
Green-tinged mass (MPO) — "chloroma"
Treatment complications
Massive cell kill releases contents; very high blast counts sludge vessels.
Tumor lysis: ↑ K⁺, ↑ phosphate, ↑ uric acid, ↓ Ca²⁺ → AKI · leukostasis: dyspnea, confusion
Fluids, allopurinol or rasburicase · hydroxyurea, leukapheresis

Mechanism — maturation arrest

Stem/progenitor mutation
→
Maturation blockedBlasts pile up
→
Marrow failureAnemia, bleeding, infection
→
InfiltrationSpleen, nodes, CNS, gums, skin

In APL, the PML-RARA fusion blocks retinoic acid signaling, so high-dose ATRA forces the promyelocytes to mature.

ALL vs AML

FEATURE
ALL
AML
Typical age
Children
Older adults
Blast markers
TdT; CD10/19 (B) or CD3/7 (T)
MPO; CD13, CD33, CD117
Auer rods
No
Yes
Key genetics
t(12;21) good · t(9;22) bad
t(15;17), t(8;21), inv(16)
Special sites
CNS, testes, mediastinum (T)
Gums (M5), DIC (M3)
Prognosis
Children: very good
Worse, especially elderly

How it's tested

COMMON CONFUSIONTdT marks immature lymphoid cells: lymphoblasts and normal thymocytes. It is absent in mature lymphomas and in AML.
THE TRAPA patient with bleeding, low fibrinogen and blasts full of Auer rods needs ATRA immediately. The DIC from APL can kill before the leukemia does.
YOUR APPROACHBlasts > 20% → TdT or MPO → age and site clues → named translocation → treatment and complication.

If you see… think…

4-year-old with petechiae and bone pain, TdT⁺ CD10⁺ blasts → B-ALL
Teen boy with a mediastinal mass and TdT⁺ CD3⁺ blasts → T-ALL
65-year-old, pancytopenia, MPO⁺ blasts with Auer rods → AML
Blasts crammed with Auer rods + DIC → APL t(15;17) — ATRA
Gum swelling + monocytic blasts → acute monocytic leukemia
Down syndrome child < 5 with megakaryoblasts → AML-M7
Adult ALL with t(9;22) → poor prognosis — add TKI
Infant ALL with KMT2A rearrangement → poor prognosis
Day 2 of induction: ↑ K⁺, ↑ uric acid, AKI → tumor lysis syndrome
AML years after treatment for another cancer → therapy-related AML